Hematology — MCQs

A 60-year-old woman complains of weakness and hematuria. Physical examination shows marked pallor, hepatosplenomegaly, and numerous ecchymoses of the upper and lower extremities. A CBC reveals a normocytic normochromic anemia, thrombocytopenia, neutropenia, and a marked leukocytosis, which is composed mainly of myeloblasts. The major clinical problems associated with this patient's condition are most directly related to which of the following?

Q269Easy

Gaisbock's syndrome refers to:

Q270Medium

Which of the following is NOT true about Multiple Myeloma?

Hematology Indian Medical PG Practice Questions and MCQs

Question 261: What is the initial treatment recommended for a newly diagnosed patient with CML?

A. Allogenic bone marrow transplantation
B. Imatinib mesylate therapy (Correct Answer)
C. TNF-a
D. IFN-a

Explanation: **Explanation:** Chronic Myeloid Leukemia (CML) is characterized by the presence of the **Philadelphia chromosome (t[9;22])**, which creates the **BCR-ABL1 fusion gene**. This gene encodes a constitutively active tyrosine kinase protein that drives uncontrolled granulocyte proliferation. **Why Imatinib is the Correct Answer:** **Imatinib mesylate** is a selective **Tyrosine Kinase Inhibitor (TKI)** that binds to the ATP-binding site of the BCR-ABL protein, effectively "switching off" the oncogenic signal [1], [2]. It is the established **first-line standard of care** for newly diagnosed CML in the chronic phase due to its high rates of complete cytogenetic response and superior safety profile compared to older therapies [1]. **Analysis of Incorrect Options:** * **A. Allogenic Bone Marrow Transplantation:** While it is the only curative treatment, it is now reserved for patients who fail TKI therapy (resistance) or progress to Blast Crisis, due to high procedural morbidity [1]. * **C. TNF-α:** Tumor Necrosis Factor-alpha has no established role in the primary management of CML. * **D. IFN-α:** Interferon-alpha was the treatment of choice before the advent of TKIs. It is now rarely used except in specific scenarios like pregnancy, where TKIs are contraindicated due to teratogenicity [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Monitoring:** The gold standard for monitoring response is **Quantitative RT-PCR** for BCR-ABL1 transcripts (Molecular Response) [1]. * **Side Effects:** Common side effects of Imatinib include **periorbital edema**, muscle cramps, and skin rashes. * **Second-generation TKIs:** Dasatinib and Nilotinib are used if Imatinib resistance develops [1]. * **T315I Mutation:** This specific mutation confers resistance to most TKIs; **Ponatinib** is the drug of choice here.

Question 262: Which of the following are clinical features characteristic of anemia?

A. Pallor of mucous membranes
B. Increased heart rate
C. Mid-systolic flow murmur
D. All of the above (Correct Answer)

Explanation: Explanation: Anemia is defined as a reduction in the oxygen-carrying capacity of the blood due to a decrease in red blood cell mass or hemoglobin concentration. The clinical features of anemia arise from two main mechanisms: **tissue hypoxia** and **compensatory cardiovascular responses.** [2] * **Option A (Pallor):** This is the most classic sign of anemia. It occurs due to reduced hemoglobin concentration in the blood and compensatory vasoconstriction of peripheral vessels to shunt blood toward vital organs. [1] It is best assessed in the conjunctiva, mucous membranes, and palmar creases. [1] * **Option B (Increased heart rate):** To maintain oxygen delivery to tissues despite low hemoglobin, the body increases cardiac output. This is achieved primarily through an increase in heart rate (tachycardia) and stroke volume, reflecting a **hyperdynamic circulation.** [1] * **Option C (Mid-systolic flow murmur):** In anemia, blood viscosity decreases. This reduced viscosity, combined with increased flow velocity (hyperdynamic state), creates turbulence across the heart valves. This typically results in a soft, mid-systolic "flow" murmur, usually heard best at the pulmonary area. Since all three features are direct clinical manifestations of the body's adaptation to anemia, **Option D** is the correct answer. **High-Yield NEET-PG Pearls:** * **Hyperdynamic State:** Anemia is a common cause of high-output heart failure. * **Koilonychia:** Spoon-shaped nails are a specific sign of Iron Deficiency Anemia. [1] * **Pica:** Craving for non-nutritive substances (ice, dirt) is highly suggestive of iron deficiency. * **Angular Stomatitis/Glossitis:** Often seen in Vitamin B12, Folate, and Iron deficiencies. [1]

Question 263: Which of the following can cause Disseminated Intravascular Coagulation (DIC)?

A. Leukemia
B. Massive transfusion
C. Abruptio placentae
D. All of the above (Correct Answer)

Explanation: Disseminated Intravascular Coagulation (DIC) is a thrombo-hemorrhagic disorder characterized by the systemic activation of the coagulation cascade, leading to widespread fibrin deposition in the microvasculature and subsequent consumption of clotting factors and platelets [1]. **Why "All of the above" is correct:** DIC is always secondary to an underlying pathology that triggers the release of tissue factor (TF) or causes endothelial injury. * **Leukemia (Option A):** Specifically, **Acute Promyelocytic Leukemia (APL/M3)** is a classic cause. The malignant promyelocytes release procoagulant granules and tissue factor, triggering massive thrombin generation. * **Massive Transfusion (Option B):** Large-volume blood replacement can trigger DIC through several mechanisms, including the introduction of procoagulant phospholipids from stored blood, citrate toxicity, and underlying trauma/hemorrhagic shock which causes endothelial damage. [2] * **Abruptio Placentae (Option C):** Obstetric complications are a leading cause of DIC. In placental abruption, there is a massive release of **tissue thromboplastin** (tissue factor) from the placenta and decidua into the maternal circulation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause overall:** Sepsis (Gram-negative organisms due to endotoxins). * **Laboratory Hallmarks:** Prolonged PT/aPTT, **decreased Fibrinogen** (best prognostic marker), thrombocytopenia, and **elevated D-dimer** (most sensitive). * **Peripheral Smear:** Presence of **Schistocytes** (fragmented RBCs) indicating microangiopathic hemolytic anemia (MAHA). * **Treatment:** Always treat the underlying cause first. Support with Platelets/FFP if bleeding occurs. In APL-induced DIC, **ATRA** (All-trans retinoic acid) is used.

Question 264: Megaloblastic anemia is seen in which of the following conditions?

A. Ileal resection (Correct Answer)
B. Crohn's disease
C. Intestinal lymphatic ectasia
D. Menetrier's disease

Explanation: **Explanation:** Megaloblastic anemia is primarily caused by a deficiency of Vitamin B12 (Cobalamin) or Folic acid [1]. The correct answer is **Ileal resection** because the **terminal ileum** is the specific site for the absorption of the Vitamin B12-Intrinsic Factor (IF) complex [2]. 1. **Why Ileal Resection is Correct:** Vitamin B12 absorption requires binding to Intrinsic Factor (produced by gastric parietal cells) and subsequent uptake by specialized receptors (cubilin) located in the terminal ileum. Surgical removal of this segment leads to a definitive malabsorption of B12, resulting in megaloblastic anemia [2]. The liver stores enough vitamin B12 for approximately 3 years, so clinical deficiency takes years to manifest even after malabsorption occurs [2]. 2. **Why Incorrect Options are Wrong:** * **Crohn’s Disease:** While Crohn’s *can* cause megaloblastic anemia if it involves the terminal ileum, it is a patchy, transmural inflammatory disease. Ileal resection is a more definitive and direct cause of absolute B12 deficiency in the context of this question. * **Intestinal Lymphatic Ectasia:** This is a protein-losing enteropathy characterized by dilated intestinal lymphatics. It leads to lymphocytopenia and hypoproteinemia (low albumin/globulins) rather than megaloblastic anemia. * **Menetrier’s Disease:** This is a hypertrophic gastropathy involving the gastric body and fundus. It causes protein loss and potentially iron deficiency anemia due to achlorhydria, but it is not a classic cause of megaloblastic anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Schilling Test:** Historically used to differentiate causes of B12 malabsorption (though rarely used now). * **Pernicious Anemia:** The most common cause of B12 deficiency globally, caused by autoimmune destruction of parietal cells [1]. * **Fish Tapeworm (*Diphyllobothrium latum*):** A classic parasitic cause of B12 deficiency. * **MCV:** In megaloblastic anemia, the Mean Corpuscular Volume is typically **>100 fL**, and peripheral smears show **hypersegmented neutrophils** (>5 lobes).

Question 265: Urgent reversal of warfarin therapy can be achieved by administration of which of the following?

A. Cryoprecipitates
B. Vitamin K and fresh frozen plasma
C. Fresh frozen plasma (Correct Answer)
D. Packed red cells

Explanation: **Explanation:** Warfarin exerts its anticoagulant effect by inhibiting the enzyme **Vitamin K Epoxide Reductase (VKOR)**, which prevents the gamma-carboxylation of Vitamin K-dependent clotting factors (**II, VII, IX, and X**) [1]. In scenarios requiring **urgent reversal** (e.g., life-threatening hemorrhage or emergency surgery), the goal is to immediately replace these deficient clotting factors. **Why Fresh Frozen Plasma (FFP) is correct:** FFP contains all coagulation factors in physiological concentrations. It provides an immediate source of factors II, VII, IX, and X, bypassing the time required for the liver to synthesize new factors. While Prothrombin Complex Concentrate (PCC) is now often preferred due to lower volume, FFP remains a standard correct answer for urgent reversal in many clinical examinations. **Why other options are incorrect:** * **Vitamin K:** While Vitamin K is the specific antidote, it acts by promoting the hepatic synthesis of new factors [1]. This process takes **6–24 hours**, making it unsuitable as a monotherapy for *urgent* reversal. * **Cryoprecipitate:** This is rich in Factor VIII, von Willebrand factor, and **Fibrinogen**. It does not contain sufficient amounts of the Vitamin K-dependent factors needed to reverse warfarin. * **Packed Red Cells:** These are used to restore oxygen-carrying capacity in anemia or active hemorrhage but do not contain clotting factors and will not correct the coagulopathy. **High-Yield Clinical Pearls for NEET-PG:** 1. **Fastest Reversal:** **Prothrombin Complex Concentrate (PCC)** is faster than FFP and is the treatment of choice if available (less volume overload). 2. **Half-life:** Factor VII has the shortest half-life (approx. 6 hours), which is why the PT/INR rises first during warfarin therapy. 3. **Monitoring:** Warfarin therapy is monitored using **PT/INR** (Extrinsic pathway) [2]. 4. **Standard Protocol:** For major bleeding, the recommendation is usually **IV Vitamin K + FFP (or PCC)**. Vitamin K is added to ensure sustained reversal once the exogenous factors from FFP are metabolized.

Question 266: In hemophiliac patients, which of the following should not be given?

A. Factor VIII concentrate
B. Cryoprecipitate
C. EACA
D. Platelet factor (Correct Answer)

Explanation: ### Explanation **Correct Option: D (Platelet factor)** **Reasoning:** Hemophilia (A and B) is a disorder of **secondary hemostasis** caused by a deficiency in clotting factors (Factor VIII or IX) [1]. It is not a disorder of primary hemostasis (platelets). Platelet factor (or platelet transfusions) is indicated for thrombocytopenia or platelet dysfunction, neither of which is present in hemophilia. Giving platelet factor provides no therapeutic benefit to a patient lacking soluble clotting factors, making it the least appropriate choice. **Analysis of Incorrect Options:** * **A. Factor VIII concentrate:** This is the **treatment of choice** for Hemophilia A [1]. Recombinant or plasma-derived concentrates provide the specific missing factor required to stabilize the fibrin clot. * **B. Cryoprecipitate:** While less commonly used today due to the risk of transfusion-transmitted infections, cryoprecipitate contains Factor VIII, von Willebrand factor, and fibrinogen [1]. It remains a viable emergency option if specific concentrates are unavailable. * **C. EACA (Epsilon-Aminocaproic Acid):** This is an **antifibrinolytic agent**. It is frequently used as an adjunctive therapy in hemophilia, particularly for mucosal bleeds (like dental extractions), as it prevents the breakdown of the fragile clots that do manage to form [1]. **Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (mostly affects males) [1]. * **Lab Findings:** Isolated **prolonged aPTT**; normal PT, normal bleeding time, and normal platelet count. * **Mixing Study:** The prolonged aPTT **corrects** when the patient's plasma is mixed with normal plasma (distinguishes deficiency from inhibitors). * **Desmopressin (dDAVP):** Useful in **Mild Hemophilia A** as it releases stored Factor VIII from Weibel-Palade bodies in endothelial cells [1]. It is ineffective in Hemophilia B.

Question 267: A 50-year-old male presents with massive splenomegaly. Which of the following conditions is NOT a likely cause of this presentation?

A. Chronic myeloid leukemia
B. Polycythemia rubra vera
C. Hairy cell leukemia
D. Aplastic anemia (Correct Answer)

Explanation: **Explanation:** The hallmark of **Aplastic Anemia** is bone marrow failure leading to peripheral pancytopenia. Crucially, the bone marrow is "empty" (hypocellular), and there is no extramedullary hematopoiesis or infiltration by malignant cells. Therefore, **splenomegaly is characteristically absent** in aplastic anemia. If a patient with pancytopenia presents with an enlarged spleen, clinicians must look for alternative diagnoses like aleukemic leukemia or hypersplenism. **Analysis of Incorrect Options:** * **Chronic Myeloid Leukemia (CML):** This is the classic cause of **massive splenomegaly**. The spleen enlarges due to the sequestration of excess mature and maturing granulocytes [1]. * **Polycythemia Rubra Vera (PRV):** Splenomegaly occurs in approximately 75% of cases due to extramedullary hematopoiesis and congestion [1]. It can become massive if the disease progresses to the myelofibrotic phase. * **Hairy Cell Leukemia (HCL):** This is a B-cell lymphoproliferative disorder where the spleen is the primary site of disease. Massive splenomegaly is a defining clinical feature, often accompanied by "dry tap" on bone marrow aspiration. **NEET-PG High-Yield Pearls:** 1. **Massive Splenomegaly (Spleen >8cm below costal margin or >1kg):** Remember the mnemonic **"CHCC"** — **C**ML, **H**airy Cell Leukemia, **C**hronic Malaria (Tropical Splenomegaly Syndrome), and **C**ala-azar (Visceral Leishmaniasis). Myelofibrosis is another top cause [1]. 2. **Pancytopenia with Splenomegaly:** Think of Cirrhosis (portal HTN), Kala-azar, or Gaucher’s disease. 3. **Pancytopenia WITHOUT Splenomegaly:** Think of Aplastic Anemia, Vitamin B12/Folate deficiency, or PNH.

Question 268: A 60-year-old woman complains of weakness and hematuria. Physical examination shows marked pallor, hepatosplenomegaly, and numerous ecchymoses of the upper and lower extremities. A CBC reveals a normocytic normochromic anemia, thrombocytopenia, neutropenia, and a marked leukocytosis, which is composed mainly of myeloblasts. The major clinical problems associated with this patient's condition are most directly related to which of the following?

A. Avascular necrosis of bone
B. Disseminated Intravascular Coagulation
C. Hypersplenism
D. Suppression of Hematopoiesis (Correct Answer)

Explanation: ### Explanation **1. Why the Correct Answer is Right:** The clinical presentation—marked pallor, hepatosplenomegaly, ecchymoses, and a CBC showing pancytopenia (anemia, thrombocytopenia, neutropenia) alongside a high myeloblast count—is diagnostic of **Acute Myeloid Leukemia (AML)** [1]. The "major clinical problems" in acute leukemia (infections, bleeding, and fatigue) are most directly caused by **Suppression of Hematopoiesis**. This occurs because the bone marrow is "packed" or infiltrated by malignant blast cells. These blasts physically crowd out and inhibit the maturation of normal hematopoietic stem cells (the "myelophthisic" effect), leading to: * **Anemia:** Causing weakness and pallor [2]. * **Thrombocytopenia:** Causing ecchymoses and hematuria [2]. * **Neutropenia:** Leading to life-threatening infections. **2. Why the Incorrect Options are Wrong:** * **A. Avascular necrosis of bone:** While seen in conditions like Sickle Cell Disease or chronic steroid use, it is not a primary clinical feature of acute leukemia. * **B. Disseminated Intravascular Coagulation (DIC):** Although DIC is a classic complication of **APML (M3 subtype)**, it is not the *most direct* cause of the overall clinical picture of bone marrow failure across all leukemias. * **C. Hypersplenism:** While the patient has splenomegaly, the cytopenias in AML are primarily due to bone marrow failure (production defect) rather than peripheral sequestration or destruction by the spleen. **3. Clinical Pearls for NEET-PG:** * **Definition of AML:** Presence of >20% myeloblasts in the bone marrow or peripheral blood [1]. * **Auer Rods:** Pathognomonic for AML (specifically the myeloblastic lineage). * **Hyperleukocytosis:** When WBC >100,000/µL, it can lead to **Leukostasis**, causing CNS or pulmonary symptoms—a medical emergency. * **Tumor Lysis Syndrome:** A common metabolic complication after starting chemotherapy in patients with high blast counts.

Question 269: Gaisbock's syndrome refers to:

A. Spurious erythrocytosis (Correct Answer)
B. Spurious thrombocytosis
C. Reactive thrombocytosis
D. Reactive erythrocytosis

Explanation: **Gaisbock’s syndrome**, also known as **Spurious Erythrocytosis** or Stress Polycythemia, is a condition characterized by an elevated hematocrit and hemoglobin concentration despite a **normal total red cell mass**. The underlying pathophysiology is a **contraction of plasma volume**, which leads to hemoconcentration. It typically affects middle-aged, hypertensive, and often overweight individuals who may be under significant emotional or physical stress. **Analysis of Options:** * **A. Spurious erythrocytosis (Correct):** This is the defining feature of Gaisbock’s syndrome [1]. Unlike Polycythemia Vera (Primary) or Hypoxia-driven erythrocytosis (Secondary), there is no actual increase in the production of red blood cells; the "increase" is relative due to low plasma volume. * **B & C. Spurious/Reactive thrombocytosis (Incorrect):** These refer to elevated platelet counts. Spurious thrombocytosis can occur due to cell fragments (e.g., schistocytes) being miscounted as platelets, while reactive thrombocytosis is an elevated count due to inflammation or iron deficiency. Neither is associated with Gaisbock’s syndrome. * **D. Reactive erythrocytosis (Incorrect):** This is a form of secondary absolute polycythemia where red cell mass is truly increased, usually in response to high erythropoietin levels (e.g., chronic hypoxia or smoking). **High-Yield Clinical Pearls for NEET-PG:** * **Key Diagnostic Feature:** Normal Red Cell Mass + Decreased Plasma Volume [1]. * **Typical Profile:** "Stressed," hypertensive, obese male smokers [1]. * **Risk Factors:** Diuretic use (which further reduces plasma volume), tobacco use, and alcohol consumption [1]. * **Management:** Focuses on lifestyle modifications (weight loss, smoking cessation) and controlling hypertension rather than phlebotomy.

Question 270: Which of the following is NOT true about Multiple Myeloma?

A. Bence Jones protein in urine
B. Hypogammaglobulinemia
C. Amyloidosis
D. Plasmacytosis < 10% (Correct Answer)

Explanation: ### Explanation **1. Why Option D is the correct (False) statement:** The diagnosis of Multiple Myeloma (MM) requires the presence of **clonal bone marrow plasma cells ≥ 10%** [1] (or biopsy-proven extramedullary plasmacytoma) along with evidence of end-organ damage (CRAB features) or specific biomarkers of malignancy. A plasmacytosis of **< 10%** is characteristic of **MGUS** (Monoclonal Gammopathy of Undetermined Significance), not Multiple Myeloma. **2. Analysis of Incorrect Options:** * **A. Bence Jones protein in urine:** These are monoclonal free light chains (kappa or lambda) filtered by the glomerulus [1]. They are a classic finding in MM and can cause "Myeloma Kidney" (cast nephropathy). * **B. Hypogammaglobulinemia:** While there is a massive increase in one specific monoclonal antibody (M-spike), the production of normal, functional immunoglobulins is suppressed [1]. This leads to secondary hypogammaglobulinemia, making patients highly susceptible to encapsulated bacterial infections. * **C. Amyloidosis:** Approximately 10–15% of MM patients develop **AL (Light Chain) Amyloidosis**, where light chains deposit in tissues, leading to organ dysfunction (e.g., macroglossia, nephrotic syndrome, or restrictive cardiomyopathy). **3. High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (Hypercalcemia), **R**enal insufficiency, **A**nemia (Normocytic), **B**one lesions (Lytic "punched-out" lesions) [1]. * **Diagnosis:** Bone marrow biopsy is the gold standard. Look for "Flame cells" or "Mott cells." * **Investigation of Choice for Bone:** Whole-body low-dose CT or MRI (X-rays are traditional; Bone scans are usually negative because there is no osteoblastic activity). * **M-Spike:** Usually IgG (>50%) followed by IgA. * **Rouleaux Formation:** Seen on peripheral smear due to increased ESR/paraproteins [1].

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Thalassemias

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Platelet Disorders

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Coagulation Disorders

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Thrombotic Disorders

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Leukemias

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Lymphomas

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Multiple Myeloma and Plasma Cell Disorders

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Myeloproliferative Neoplasms

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Hematopoietic Stem Cell Transplantation

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Hematology — MCQs

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